HOOKWORMS

A. duodenale (Old World hookworm) and N. americanus (New World hookworm) affect approximately one quarter of the world’s population. Both species have a worldwide distribution. A. duodenale is most common in areas bordering the Mediterranean Sea, southeast Asia, India, Australia, and Oceania. N. americanus is most common in the southern United States, Central and South America, Africa, southeast Asia, and the South Pacific.

Hookworm larvae inhabit moist, shady soil. Infection generally occurs in areas where human feces are used as fertilizer. Barefoot children and agricultural workers are at highest risk of hookworm infection. Although N. americanus is acquired exclusively by skin penetration, A. duodenale may be acquired percutaneously, orally, and in a transmammary fashion.

Life cycle. The life cycles of both worms are identical. Humans are infected when filariform larvae inhabiting contaminated soil penetrate the skin and pass through the venous system to the lungs. Larvae migrate from the lungs up through the trachea and into the esophagus where they are swallowed and enter the stomach and small intestine. In the upper small intestine, particularly the jejunum, the young worms attach to the intestinal wall and mature, copulate, and produce eggs. The female worm produces 10,000 to 20,000 eggs per day. The eggs are passed in the feces to warm, moist soil where they rapidly develop and hatch in 1 to 2 days. The newly hatched rhabditiform larvae feed on bacteria in the soil and become infectious filariform larvae in 7 to 10 days.

Clinical manifestations. The clinical manifestations of hookworm infection are related to the life cycle of the worm. Initial skin penetration causes a localized pruritic rash accompanied by papulovesicular eruptions. This symptom complex is called “ground itch” and is more common in N. americanus infection. As larvae pass through the lungs, bronchitis or pneumonitis may occur.

Abdominal pain, nausea, vomiting, pica, and anorexia can occur when worms enter the intestinal tract. Diarrhea with mucus and blood may occur, while some patients may complain of constipation. The hallmark of hookworm infection is iron deficiency anemia. This occurs as worms attach to the intestinal mucosa and engorge with blood, as well as through continued seepage of blood from previous attachment sites. Daily blood loss secondary to N. americanus is estimated to be 0.03 mL/d per worm, and that of A. duodenale is estimated to be 0.15 mL/d per worm. Chronic fatigue, weakness, lassitude, and depression often develop as a consequence of anemia. More severe complications of the anemia include cardiomyopathy, tachycardia, and failure to thrive. The anemia of hookworm infection is distinctly uncommon in the United States, but is common in third world countries. A protein-losing enteropathy leading to hypoalbuminemia and facial and pedal edema occurs although the pathogenesis remains controversial.

Diagnosis, treatment, and prevention. The diagnosis of hookworm infection is based on the identification of eggs in the stool. Hookworm eggs are ovoid with bluntly rounded ends and possess a colorless, thin hyaline shell. It is difficult and impractical to attempt to differentiate the eggs of the two hookworm species microscopically, as they appear identical, and treatment for both species is the same.

The drug of choice for hookworm infection is mebendazole, 100 mg BID for 3 days. The adult and pediatric doses of mebendazole are the same. Pyrantel pamoate at a dosage of 11 mg/kg (maximum 1 g) for 3 days or a single 400-mg dose of albendazole is also effective.

Oral iron therapy should be given to all patients with iron deficiency anemia, and a diet rich in protein and iron should be recommended to all patients. Pregnant women with hookworm infection and iron deficiency anemia should be initially treated with iron replacement, and anthelminthic therapy should be reserved for after delivery.

Prevention of hookworm infection can be achieved through improvement in methods of rural sanitation and personal hygiene. Educating the public to the importance of using latrines and wearing proper footwear is vital to the control of this parasite.

A. MARINA

Anisakiasis, or herringworm disease, was first identified in 1966. Although the majority of cases have been reported in Japan, Holland, and the Pacific coast of South America, anisakiasis has a worldwide distribution. Infection with this nematode must be considered wherever raw fish is consumed. The popularity of sushi restaurants in the United States and Japan, herring in Holland, and ceviche in South America has increased public awareness of this condition.

Life cycle. The life cycle of A. marina is not completely known. The adult worm inhabits the intestinal tracts of marine mammals and birds. Eggs are passed in the host feces and the larvae hatch in the sea. The larvae are taken up by various crustaceans and develop into an infective stage. The crustaceans enter the food chain and are eaten by fish. When an infected fish is eaten by a human, larvae burrow inside the human stomach or intestine.

Clinical manifestations. Anisakiasis may cause colicky abdominal pain, nausea, vomiting, and fever. Occasionally, pain may be so severe as to mimic peritonitis or appendicitis and lead to surgical intervention. A. marina is an invasive organism and may cause ulceration, abscess, eosinophilic granuloma, or intestinal perforation. These symptoms may be mistaken for Crohn’s disease.

Diagnosis, treatment, and prevention. The diagnosis of anisakiasis is difficult to make and should be considered whenever abdominal symptoms follow ingestion of raw saltwater fish. The diagnosis is usually made at the time of laparoscopy or endoscopy. Occasionally, the patient will present vomiting worms.

There is no proven therapy for anisakiasis. If the diagnosis is made prior to surgical intervention, treatment with thiabendazole can be tried. Anisakiasis can be prevented with proper handling of saltwater fish. Fish should be cooked for at least 10 minutes at 60°C or frozen to –20°C for 60 hours.

C. PHILIPPINENSIS

Intestinal capillariasis caused by C. philippinensis, a nematode related to T. trichiura, was first described in the northern Philippines in the 1960s. Since this initial report, more than 1000 cases occurring in the Philippines, Thailand, Japan, Korea, Indonesia, Taiwan, Iran, Egypt, Spain, and Colombia have been reported.

Life cycle. The life cycle of C. philippinensis includes fish as intermediate hosts and fish-eating birds as probable hosts. Fish-eating birds ingest fish infected with larvae, and the larvae become adults in the bird’s GI tract. Eggs pass from the bird’s feces into freshwater, where they embryonate. Embryonated eggs are ingested by freshwater fish and develop into larvae in the fish intestine. Humans acquire the infection by eating raw, small, freshwater fish, crustaceans, or snails. Adult worms inhabit the small intestine, predominantly the jejunum.

Clinical manifestations. The most common presenting symptoms are anorexia, nausea, vomiting, diarrhea, borborygmus, and abdominal pain. Chronic infection can lead to severe malabsorption with an accompanying protein-losing enteropathy, electrolyte abnormalities, steatorrhea, and edema. Untreated infection has a mortality rate of about 10%.

Diagnosis, treatment, and prevention. Diagnosis is based on the identification of eggs in the feces of a symptomatic patient. Asymptomatic infection and autoinfection can occur. The treatment of choice in the American literature is 200 mg of mebendazole BID for 20 days. The pediatric dose is the same. The treatment of choice in the Philippines, where the disease is endemic, is 200 mg of albendazole BID for 10 days. Thiabendazole, 25 mg/kg per day given in two dosages for 30 days, is a less effective alternative. In addition to anthelminthic therapy, electrolyte replacement and an antidiarrheal agent should be given. C. philippinensis can be prevented by avoiding the ingestion of raw or partially cooked freshwater fish, snails, and crustaceans.

E. VERMICULARIS

E. vermicularis has a worldwide distribution and is the most common intestinal nematode seen in North America. This parasite most commonly affects children 5 to 14 years of age and is more common in temperate and cold climates, secondary to less frequent bathing and changing of undergarments. Transmission within families is common, and high rates have been reported in homosexual men. Despite its high prevalence, pinworm rarely causes severe disease.

Life cycle. The life cycle takes place entirely within the lumen of the GI tract. Transmission of pinworm occurs via direct infection from the anal canal to the mouth by finger contamination, via airborne eggs that dislodge from bed linens and clothes, and via contaminated dust containing embryonated eggs (fomites). After ingestion, eggs hatch in the stomach and small intestine and migrate to the ileum, cecum, appendix, and ascending colon where they attach to the mucosa. The worms mate in these areas and the gravid female becomes engorged with eggs. During the night, the gravid females migrate out of the anus and deposit mature eggs in the perianal and perineal regions by a process known as oviposition.

Clinical manifestations. The most common symptom of pinworm infection is pruritus ani; however, most pinworm infections are asymptomatic. Other symptoms that have been described include abdominal pain, irritability, restlessness, insomnia, and fatigue. Some children develop feelings of shame and guilt that may manifest as anorexia, depression, enuresis, or emotional instability. Pinworm infection has been linked to appendicular pain and chronic inflammation; however, there appears to be no relationship with acute appendicitis. Ulcerations of colonic mucosa have been described in areas of pinworm infestation.

Complications of pinworm infection include secondary bacterial dermatitis and folliculitis. Vulvovaginitis may occur with worm migration to the vagina.

Diagnosis, treatment, and prevention. Pinworm infection is diagnosed by identifying the adult worm or eggs from the perineum. This is usually done at night as the female passes through the anal canal to deposit her eggs. Alternatively, a strip of adhesive tape can be applied sticky side down to the uncleaned perianal area in the morning prior to defecation or bathing in order to capture characteristic eggs. The adhesive side of the tape is then placed onto a glass slide, and the slide is examined for eggs.

E. vermicularis is quite responsive to drug therapy, although the relapse rate is high. In addition to drug therapy, proper personal hygiene, sterilization of bed linens, and dust removal must be performed. The treatment of choice for pinworm is a single dose of pyrantel pamoate, 11 mg/kg (maximum 1 g), with another dosage given in 2 weeks. A single dose of either 100 mg of mebendazole or 400 mg of albendazole, with a repeat dosage given in 2 weeks, is adequate alternative therapy. The entire family should be treated simultaneously.

Prevention of pinworm infection depends on maintaining adequate personal hygiene and clean living quarters. Hand washing and fingernail cleaning should be done as much as possible. Frequent washing of the toilet seat should be performed. Linens or clothing should not be shaken prior to washing. Thumb sucking, fingernail biting, and anal scratching should be discouraged.

S. STERCORALIS

S. stercoralis is a soil-dwelling nematode with a worldwide distribution that is commonly found in the tropics and subtropics. In temperate climates, S. stercoralis is commonly found in the setting of group homes, mental hospitals, prisons, and settlements of refugees from endemic areas. As a result of autoinfection, strongyloidiasis may be found years later in veterans from the wars in Vietnam, Korea, and World War II.

Life cycle. The life cycle of S. stercoralis is more complicated than that of other nematodes as it has the unique ability to perpetuate itself in both the human host and soil. Under appropriate soil conditions, free living worms produce rhabditiform larvae that become infective filariform larvae after several months. The filariform larvae penetrate the skin and enter the lymphatic and venous systems where they are carried through the heart into the lungs. In the lungs, the larvae penetrate the alveolar spaces and migrate up the trachea and into the esophagus where they are swallowed and migrate to the duodenum and upper jejunum. The larvae mature into adult worms in the small intestine and lay eggs, which are either expelled in feces or take up residence in the colon. The rhabditiform larvae in the colon transform into filariform larvae, penetrate the bowel wall, and complete the life cycle. Other rhabditiform larvae may transform into filariform larvae in fecal matter that adheres to the skin, penetrate the skin in that area, and complete the life cycle.

Clinical manifestations. The majority of acute S. stercoralis infections are asymptomatic. Pulmonary symptoms such as cough, wheezing, or the development of Löffler’s syndrome may occur as larvae invade the lungs. Acute GI symptoms include epigastric pain and diarrhea. Pseudo-obstruction, bleeding gastric ulcer, colonic ulceration, and concomitant enteric bacterial infections may occur with S. stercoralis infection.

Chronic strongyloidiasis may be asymptomatic, although patients can present with lower abdominal cramping, biliary colic, intermittent or persistent diarrhea, pruritus ani, or malabsorption.

Hyperinfection or overwhelming strongyloidiasis may develop in patients with impaired host-defense systems due to corticosteroid therapy.

Diagnosis, treatment, and prevention. The diagnosis of strongyloidiasis is made by identifying rhabditiform larvae in the stool. The peripheral eosinophil count is markedly elevated in acute disease (up to 85% of the white blood cell count), moderately elevated in chronic disease, and absent in overwhelming infection.

The treatment of choice for strongyloidiasis is 25 mg/kg per day of thiabendazole BID (maximum 3 g/d) for 2 days. Ivermectin, 200 mg/kg per day given for 2 days, has also been shown to be effective. Preventive measures include the sanitary disposal of human feces and the wearing of appropriate footwear.

T. TRICHIURA

T. trichiura, or whipworm, is found in areas of poor sanitation and overcrowding, primarily in the tropics and subtropics. In the United States, whipworm is seen mostly in immigrants from tropical regions and in rural areas of the southeast.

Life cycle. T. trichiura is transmitted by ingestion of embryonated eggs from feces-contaminated soil. Eggs hatch and produce larvae that attach to the mucosa of the small intestine and mature. After a period of maturation of up to 3 months, the worms migrate to the colon and attach to the colonic mucosa, predominantly in the cecum. The worms produce eggs that are excreted in the feces.

Clinical manifestations. Symptoms of whipworm infection are dependent upon worm load. Light infections (fewer than 100 worms) are the most common and are usually asymptomatic. Lower abdominal pain, nausea, flatulence, weight loss, and diarrhea may occur with light infection. Infections with increased worm load (hundreds of worms) may cause periumbilical pain, vomiting, anorexia, pica, and dysentery. Rectal prolapse, although uncommon in the United States, is occasionally seen in third world nations. Whipworm has been reported to simulate rectal Crohn’s disease. Iron deficiency anemia, growth retardation, and clubbing have all been noted in T. trichiura infection. Severe trichuriasis is frequently associated with a secondary intestinal infection such as shigellosis, amebiasis, ascariasis, or strongyloidiasis.

Diagnosis, treatment, and prevention. The diagnosis of T. trichiura is made by identifying eggs in the stool, which are bile-stained and have a characteristic mucus plug on each end. Worms can occasionally be seen on proctosigmoidoscopy or embedded in prolapsed rectal mucosa. Eosinophilia is uncommon in T. trichiura infection and when present may indicate massive or concomitant infection.

The treatment of choice for T. trichiura infection is 100 mg of mebendazole BID for 3 days. The dose is the same in adults and children. Albendazole, given at a single dosage of 400 mg daily is an alternative therapy. Prevention of T. trichiura infection requires proper personal hygiene and adequate facilities for feces disposal.

A. LUMBRICOIDES

A. lumbricoides is the most common helminthic infection in humans and is found on all continents, with the exception of Australia and Antarctica. It is most common in Asia as a source of disease. The organism is found in areas of poor hygiene and especially in places where human feces are utilized as fertilizer. A. lumbricoides may affect all age groups, but is most common in children. Contamination of soil in playgrounds and utilization of garbage as toys contribute to the increased incidence in this patient population.

Life cycle. An adult A. lumbricoides is a creamy white worm measuring 15 to 35 cm in length that typically inhabits the jejunum and middle ileum. The female lays approximately 200,000 eggs per day that are passed in host feces. The ova require 2 weeks of incubation in soil for maturation before becoming infective. Infective eggs must be ingested for human infection to occur. This may occur from the ingestion of contaminated soil, vegetables, or water. After ingestion, the ova hatch in the duodenum. The resulting larvae then enter the portal circulation and pass to the lungs, where they migrate across pulmonary and capillary beds, up the respiratory tree, and are swallowed as mature worms. These worms live intraluminally but may migrate into the ampulla of Vater, entering the common bile duct and/or pancreatic duct.

Clinical manifestations. The clinical manifestations of A. lumbricoides infection can be divided into two clinical stages: larval migration and adult worm infection.

As larvae migrate through the venules, they may produce hepatitis, although it is rare. Larvae migrating through the lungs may cause cough, hemoptysis, dyspnea, pulmonary edema, or Löffler’s syndrome.

Symptoms of adult worm infection of the GI tract are dependent upon worm load. Light infections tend to be asymptomatic although patients may complain of vague abdominal pain, anorexia, or malaise. Infections with multiple worms may lead to more serious complications, such as intestinal obstruction or perforation.

Intestinal obstruction typically presents with nausea, vomiting, and colicky abdominal pain. A palpable abdominal mass that changes in size and location on serial examinations is typical of ascariasis. Obstruction is most common at the ileocecal valve. Untreated intestinal obstruction can lead to volvulus, perforation, and peritonitis. The incidence of intestinal obstruction is approximately 2 in 1000 cases in children.

A. lumbricoides may migrate up the common bile duct or pancreatic duct and cause cholangitis or pancreatitis; in addition, it may migrate into the appendix, leading to appendicitis. Tapeworms also cause intussusception of the small intestine.

Diagnosis, treatment, and prevention. The diagnosis of ascariasis is based on observation of an adult worm passed in the stool. The identification of ova in the host stool or the vomiting of worms is also diagnostic of A. lumbricoides infection. Eosinophilia is common.

The treatment of choice for A. lumbricoides is 100 mg of mebendazole BID for 3 days. Albendazole, 400 mg given once a day for 2 days, or a single 11-mg/kg dose of pyrantel pamoate (maximum 1 g) are alternative therapies.

Intestinal obstruction can generally be treated conservatively with IV fluids and nasogastric suction, followed by the administration of anthelminthic therapy via a nasogastric tube. Obstruction associated with fever or a distended abdomen usually requires surgical intervention.

The prevention of A. lumbricoides infection is dependent upon improving sanitary conditions and personal hygiene in areas of high prevalence.

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